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10.1038/srep27112 http://scihub22266oqcxt.onion/10.1038/srep27112 C4895243!4895243 !27271556     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27271556 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Sci+Rep 2016 ; 6 (ä): 27112 Nephropedia Template TP {{tp|p=27271556 |t=2016. Lysosomal protease cathepsin D; a new driver of apoptosis during acute kidney injury |pdf=|usr=}}{{27271556 }} gab.com Text Lysosomal protease cathepsin D; a new driver of apoptosis during acute kidney injury JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27271556 #FOAvip Acute kidney injury (AKI) is an abrupt reduction in kidney function caused by different pathological processes. It is associated with a significant morbidity and mortality in the acute phase and an increased risk of developing End Stage Renal Disease. Despite the progress in the management of the disease, mortality rates in the last five decades remain unchanged at around 50%. Therefore there is an urgent need to find new therapeutic strategies to treat AKI. Lysosomal proteases, particularly Cathepsin D (CtsD), play multiple roles in apoptosis however, their role in AKI is still unknown. Here we describe a novel role for CtsD in AKI. CtsD expression was upregulated in damaged tubular cells in nephrotoxic and ischemia reperfusion (IRI) induced AKI. CtsD inhibition using Pepstatin A led to an improvement in kidney function, a reduction in apoptosis and a decrease in tubular cell damage in kidneys with nephrotoxic or IRI induced AKI. Pepstatin A treatment slowed interstitial fibrosis progression following IRI induced AKI. Renal transplant biopsies with acute tubular necrosis demonstrated high levels of CtsD in damaged tubular cells. These results support a role for CtsD in apoptosis during AKI opening new avenues for the treatment of AKI by targeting lysosomal proteases. Twit Text FOAVip Lysosomal protease cathepsin D; a new driver of apoptosis during acute kidney injury ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27271556 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27271556 #FOAvip English Wikipedia <ref>{{Cite pmid|27271556 }}</ref> Lysosomal protease cathepsin D; a new driver of apoptosis during acute kidney injury #MMPMID27271556 Cocchiaro P ; Fox C ; Tregidgo NW ; Howarth R ; Wood KM ; Situmorang GR ; Pavone LM ; Sheerin NS ; Moles A Sci Rep 2016[Jun]; 6 (ä): 27112 PMID27271556 show ga Acute kidney injury (AKI) is an abrupt reduction in kidney function caused by different pathological processes. It is associated with a significant morbidity and mortality in the acute phase and an increased risk of developing End Stage Renal Disease. Despite the progress in the management of the disease, mortality rates in the last five decades remain unchanged at around 50%. Therefore there is an urgent need to find new therapeutic strategies to treat AKI. Lysosomal proteases, particularly Cathepsin D (CtsD), play multiple roles in apoptosis however, their role in AKI is still unknown. Here we describe a novel role for CtsD in AKI. CtsD expression was upregulated in damaged tubular cells in nephrotoxic and ischemia reperfusion (IRI) induced AKI. CtsD inhibition using Pepstatin A led to an improvement in kidney function, a reduction in apoptosis and a decrease in tubular cell damage in kidneys with nephrotoxic or IRI induced AKI. Pepstatin A treatment slowed interstitial fibrosis progression following IRI induced AKI. Renal transplant biopsies with acute tubular necrosis demonstrated high levels of CtsD in damaged tubular cells. These results support a role for CtsD in apoptosis during AKI opening new avenues for the treatment of AKI by targeting lysosomal proteases. |Acute Kidney Injury/drug therapy/etiology/*metabolism/physiopathology [MESH] |Animals [MESH] |Apoptosis [MESH] |Cathepsin D/*metabolism [MESH] |Cell Line [MESH] |Disease Models, Animal [MESH] |Folic Acid/adverse effects [MESH] |Humans [MESH] |Kidney Function Tests [MESH] |Kidney Tubules/*cytology/drug effects/enzymology [MESH] |Male [MESH] |Mice [MESH] |Nephrosis/chemically induced/*complications/drug therapy/enzymology [MESH] |Pepstatins/administration & dosage/pharmacology [MESH] |Reperfusion Injury/*complications/drug therapy [MESH]Lysosomal protease cathepsin D; a new driver of apoptosis during acute(epmc).pdf DeepDyve Pubget Overpricing